A functional variant in the promoter region regulates the C-reactive protein gene and is a potential candidate for increased risk of atrial fibrillation.

OBJECTIVES: In a large population-based cohort, the level of C-reactive protein (CRP) in patients at baseline predicts an increased risk of future development of atrial fibrillation (AF). The mechanism of this increased risk is unknown. Furthermore, both the molecular effects of CRP on atrial myocytes and fibroblasts and whether genetic variants in the CRP gene predispose to AF are also unknown. METHODS: A genetic association study between CRP gene polymorphisms and AF was performed in two independent populations (I: 100 AF patients and 101 controls; II: 348 AF patients and 356 controls), with functional studies to elucidate the mechanism of association. RESULTS: Three polymorphisms (T-861C, A-821G and C-390A/C-390T) were found in the 1-kb promoter of CRP. A triallelic polymorphism (C-390A/C-390T) captured all haplotype information and determined the CRP gene promoter activity and the plasma CRP level, and was in nearly complete linkage disequilibrium with G1059C polymorphism in exon 2. The -390A variant was associated with a higher CRP gene promoter activity, a higher plasma CRP level and a higher risk of AF. Patients with AF also had a higher plasma CRP level than controls. CRP significantly increased the inward L-type calcium current in atrial myocytes with no changes in other ionic currents. CRP did not affect the expressions of type I alpha 1 (COL1A1), type III alpha 1 (COL3A1) and type 1 alpha 2 (COL1A2) procollagens in atrial fibroblasts. CONCLUSION: A CRP gene promoter triallelic polymorphism was associated with CRP gene promoter activity, determined the plasma level of CRP, and predicted the risk of AF. The mechanism of this may be via augmention of calcium influx by CRP in atrial myocytes, but not because of atrial fibrosis.

Differential association of proinflammatory cytokines with left ventricular diastolic dysfunction in subjects with and without continuous ambulatory peritoneal dialysis.

BACKGROUND AND AIMS: The association between inflammation and left ventricular (LV) diastolic dysfunction in continuous ambulatory peritoneal dialysis (CAPD) and non-CAPD patients is not established. The objective of this study was to test the above association and whether inflammation interacts with CAPD to increase LV diastolic dysfunction risks. METHODS AND RESULTS: 120 subjects with normal creatinine levels and 101 CAPD patients were recruited. Echocardiographic parameters were assessed in all patients. The participants were classified as having LV diastolic dysfunction by echocardiographic findings including mitral inflow E/A ratio < 1, deceleration time > 220 cm/s, or decreased peak annular early diastolic velocity in tissue Doppler imaging. Blood was sampled at the baseline for measurement of inflammation markers, including tissue necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Subjects with LV diastolic dysfunction had higher proinflammation cytokines levels in both groups. Inflamed markers correlated significantly with echocardiography parameters for LV diastolic dysfunction in patients receiving CAPD. In a multivariate regression analysis adjusting for all the factors associated with LV diastolic dysfunction, inflammation is still significantly associated with left ventricular diastolic dysfunction (TNF-alpha, OR: 2.6, 95% CI: 2.0-3.35, p < 0.001; IL-6, OR: 1.26, 95% CI: 1.25-1.26, p = 0.01). In addition, the interaction of CAPD and inflammation significantly contributed to the development of LV diastolic dysfunction (CAPD∗ TNF-α: OR: 1.45, 95% CI: 1.13-1.79, P = 0.004). CONCLUSION: We found inflammation plays a vital role for LV diastolic dysfunction especially in CAPD patients. A synergistic effect between CAPD and inflammation, especially TNF-α, would further aggravate LV diastolic dysfunction.

Renin-angiotensin system gene polymorphisms and diastolic heart failure.

BACKGROUND: Diastolic heart failure (DHF) refers to an abnormality of diastolic distensibility, filling or relaxation of the left ventricle. The genetic study of DHF is scarce in the literature. The association of renin-angiotensin system (RAS) and DHF are well known. We hypothesized that RAS genes might be the susceptible genes for DHF and conducted a case-control study to prove the hypothesis. MATERIALS AND METHODS: A total of 1452 consecutive patients were analysed and 148 patients with a diagnosis of DHF confirmed by echocardiography were recruited. We had two control populations. The first controls consisted of 286 normal subjects while the second were 148 matched controls selected on a 1-to-1 basis by age, sex, hypertension, diabetes and medication use. The angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism; multilocus polymorphisms of the angiotensinogen gene; and the A1166C polymorphisms of the angiotensin II type I receptor (AT(1)R) gene were genotyped. RESULTS: In a single-locus analysis, the odds ratios (ORs) for DHF were significant with the ACE DD genotype and the AT(1)R 1166 CC plus AC genotype. In addition, the concomitant presence of ACE DD and AT(1)R 1166 CC/AC genotypes synergistically increased the predisposition to DHF. CONCLUSIONS: Genetic variants in the RAS genes may determine an individual's risk to develop DHF. There is also a synergistic gene-gene interaction between the RAS genes in the development of DHF.

Aminoguanidine prevents fructose-induced deterioration in left ventricular-arterial coupling in Wistar rats.

BACKGROUND AND PURPOSE: Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that prevents the fructose-induced arterial stiffening in male Wistar rats. Our aims were to examine whether AG produced benefits on the left ventricular (LV)-arterial coupling in fructose-fed (FF) animals in terms of the ventricular and arterial chamber properties. EXPERIMENTAL APPROACH: Rats given 10% fructose in drinking water (FF) were daily treated with AG (50 mg x kg(-1), i.p.) for 2 weeks and compared with the untreated FF group. In anaesthetised rats, LV pressure and ascending aortic flow signals were recorded to calculate LV end-systolic elastance (E(es), an indicator of myocardial contractility) and effective arterial volume elastance (E(a)). The optimal afterload (Q(load)) determined by the ratio of E(a) to E(es) was used to measure the coupling efficiency between the left ventricle and its vasculature. KEY RESULTS: There was a significant interaction between fructose and AG in their effects on E(a). Fructose loading significantly elevated E(a) and AG prevented the fructose-derived deterioration in arterial chamber elastance. Both fructose and AG affected E(es) and Q(load), and there was an interaction between fructose and AG for these two variables. Both E(es) and Q(load) exhibited a decline with fructose feeding but showed a significant rise after AG treatment in the FF rats. CONCLUSIONS AND IMPLICATIONS: AG prevented not only the contractile dysfunction of the heart caused by fructose loading, but also the fructose-induced deterioration in matching left ventricular function to the arterial system.

Differential lipogenic effects of cilostazol and pentoxifylline in patients with intermittent claudication: potential role for interleukin-6.

Cilostazol, a novel oral phosphodiesterase inhibitor, has shown consistent improvement in exercise tolerance in patients with intermittent claudication (IC). In addition to this effect, cilostazol has previously been shown to have beneficial effects on the dyslipidemia, i.e., combination of high triglycerides with low high-density-lipoprotein cholesterol (HDL-C) levels. Interleukin-6 (IL-6) suppresses the activity of lipoprotein lipase, which modulates the metabolism of triglycerides and HDL-C. To determine whether a reduction of IL-6 contributes to the improvement of lipid profiles, we prospectively investigated the effect of cilostazol (n=16, 100 mg, twice daily) on the changes of lipid profiles and on the association with the changes of IL-6 compared with those of pentoxifylline (n=16, 400 mg, bid) in patients with IC. After eight weeks of administration of cilostazol to patients with IC, walking distances were increased, associated with a 29% decrease in plasma triglycerides and a 13% increase in HDL-C. No significant changes of lipid profiles in the pentoxifylline and placebo groups were observed although a similar improvement in walking distances was achieved in the pentoxifylline group. IL-6 levels were significantly reduced in patients receiving cilostazol as compared with those receiving placebo or pentoxifylline. The cilostazol-induced changes in the IL-6 were positively related to those of triglycerides in the cilostazol group (r=0.63, P<0.05) and negatively related to those of HDL-C (r=-0.55, P<0.05). These findings suggest that in addition to consistent improvement of exercise tolerance, cilostazol may improve lipid profiles by reducing IL-6 release. However, pentoxifylline did not affect lipid profiles although a similar improvement of maximal walking distance (MWD) was achieved.

Molecular variant M235T of the angiotensinogen gene is associated with essential hypertension in Taiwanese.

OBJECTIVE: To examine the association of the molecular variants of the angiotensinogen (AGT) gene with essential hypertension in Taiwanese. METHODS: We conducted a case-control study concerning 151 subjects, 102 hypertensives and 49 normotensives. We created a rapid mini-sequencing method based on dye-terminator cycle sequencing to simultaneously detect the M235T and T174M variants of the AGT gene for each subject. RESULTS: The genotype and allele distribution of the M235T variant differed significantly in hypertensives and normotensives (chi 2 = 11.106, P = 0.004 and chi 2 = 6.453, P = 0.011, respectively), whereas those of the T174M variant did not differ (chi 2 = 0.004, P = 0.998 and chi 2 = 0.032, P = 0.858, respectively). The odds ratio for hypertension was 3.64 (95% confidence interval 1.56-8.49) for subjects with the C/C genotype of the M235T variant compared with other genotypes of 2.87 (95% confidence interval 1.76-4.68) for those carrying allele C versus those carrying allele T. CONCLUSION: The molecular variant M235T, but not T174M, of the AGT gene is associated significantly with essential hypertension in this Taiwanese population. The genotype C/C or allele C is a risk factor for hypertension. The underlying mechanism of this association needs to be elucidated further.

Electrophysiologic manifestations of the excitable gap of orthodromic atrioventricular reciprocating tachycardia demonstrated by single extrastimulation.

To assess the electrophysiologic characteristics of the excitable gap, 12 patients with orthodromic atrioventricular (AV) reciprocating tachycardia were studied. During tachycardia, 8 patients used a left-sided and 4 patients a right-sided anomalous bypass tract for retrograde conduction. QRS complex-synchronized single extrastimuli were delivered from high right atrium, right ventricular apex and coronary sinus, respectively, scanning the whole cycle length of tachycardia. An excitable gap was determined to be present if tachycardia resetting or tachycardia termination occurred. The duration of the excitable gap varied among different pacing sites and occupied 0 to 48% (mean 17 +/- 16) of basic tachycardia cycle length (240 to 480 ms, mean 327 +/- 70). Three patterns of tachycardia resetting were observed: the sum of coupling interval and return cycle being (1) less than a fully compensatory pause in 12 of 12 patients, (2) more than a fully compensatory pause in 5 of 12 patients and (3) equal to a fully compensatory pause in 2 of 12 patients, depending on extent of AV nodal conduction delay exhibited in return cycle. Tachycardia termination was possible when extrastimuli were delivered from right ventricular apex and coronary sinus but not from high right atrium, and only when basic tachycardia cycle length was greater than or equal to 290 ms in 7 of 12 patients. Tachycardia termination was accounted for by development of orthodromic conduction block in AV node in 7 of 7 patients and in bypass tract in 2 of 7 patients. Therefore, site of extra-stimulation and basic tachycardia cycle length affect electrophysiologic manifestations of excitable gap. Further, functional properties of the AV node influence patterns of tachycardia resetting and are primarily responsible for tachycardia termination during programmed single extrastimulation.

Relation of Chlamydia pneumoniae infection in Taiwan to angiographically demonstrated coronary artery disease and to the presence of acute myocardial infarction or unstable angina pectoris.

Reports of the association of Chlamydia pneumoniae (C. pneumoniae) infection with coronary artery disease (CAD) are scarce in the Oriental population. We therefore conducted a case-control study to explore this issue in Taiwan. There were 242 consecutive subjects (166 men and 76 women) who underwent cardiac catheterization at the National Taiwan University Hospital Cardiac Catheterization Laboratory. Patients with CAD (n = 156) had > or = 1 coronary artery lesion of > 50% diameter stenosis on angiography. Controls (n = 86) had no demonstrable CAD angiographically. Antibodies to C. pneumoniae were tested by using an enzyme-linked immunosorbent assay. The prevalence of antibodies to C. pneumoniae was as follows: immunoglobulin-G (IgG), 50% (122 of 242 patients); immunoglobulin-A (IgA), 72% (176 of 242 patients); and either IgG or IgA, 79% (192 of 242 patients ). The odds ratio (OR) for CAD with either IgG or IgA was 1.4 (95% confidence interval [CI] 0.7 to 2.7, p = 0.31). After adjusting for the known CAD risk factors, the OR decreased to 0.8 (95% CI 0.3 to 2.1, p = 0.60). The OR for unstable angina or acute myocardial infarction with the presence of either IgG or IgA was 0.5 (95% CI 0.2 to 1.1, p = 0.08) and 0.4 ( 95% CI 0.1 to 1.0, p = 0.049) after adjusting for other risk factors. These results suggest a high prevalence of C. pneumoniae infection in Taiwan. However, C. pneumoniae infection is not associated with angiographically documented CAD, and, in contrast, is a negative predictor for the development of acute coronary syndromes.

Percutaneous balloon pericardiotomy for patients with recurrent pericardial effusion: using a novel double-balloon technique with one long and one short balloon.

Percutaneous balloon pericardiotomy is effective and less invasive for the treatment of recurrent pericardial effusion. This study suggests that the double-balloon method with 1 longer and 1 shorter balloon is the procedure of choice for percutaneous balloon pericardiotomy.

Ruptured aneurysms of the sinus of Valsalva in Oriental patients.

Between 1964 and 1987, a total of 57 cases of ruptured aneurysm of the sinus of Valsalva underwent surgical correction at the National Taiwan University Hospital. This represents 0.96% of all cardiac operations. The origin of ruptured aneurysm of the sinus of Valsalva was the right coronary sinus in 46, the noncoronary sinus in nine, and the left coronary sinus in two. The aneurysms ruptured into the right ventricle in 44, into the right atrium in 11, into the left ventricle in one, and into both the right ventricle and right atrium in one. Associated congenital cardiac anomalies included ventricular septal defect in 30 patients, aortic regurgitation in 20, and infundibular pulmonic stenosis and coarctation of the aorta in one each. Operative death occurred in two patients (3.5%) and one patient had a successful reoperation. The remainder did well following surgery. To compare the differences between Oriental and Western countries in ruptured aneurysm of the sinus of Valsalva, 361 cases (195 Oriental patients versus 166 Western) were collected from the literature. Analyses of these cases revealed that ruptured aneurysm of the sinus of Valsalva in Oriental patients compared with Western series is characterized by a higher incidence (5 times), more aneurysms originating from the right coronary sinus (87.9% versus 63.6%), more aneurysm rupturing into the right ventricle (84.2% versus 56.6%), a higher incidence of association with ventricular septal defect (mainly supracristal) (59.0% versus 34.6%), less incidence of association with other congenital cardiac abnormalities (4.1% versus 21.5%), very few instances of rupturing into cardiac chambers other than the right ventricle and right atrium, and less incidence of occurrence in the extremities of ages (the youngest was 7 years in Oriental patients versus 11 months in the Western series). In other words, ruptured aneurysm of the sinus of Valsalva in Oriental patients is more or less a simple and uniform disease entity in contrast to the more diverse and protean pathologic profiles encountered in Western series. However, both Oriental patient and Western patient series have similar incidences of combination with aortic regurgitation (24.6% versus 20.0%), with 40.4% of Oriental patients and 60.6% of Western patients presenting with intact ventricular septum. Therefore the pathogenetic mechanisms of ruptured aneurysm of the sinus of Valsalva may at the same time contribute to the development of aortic regurgitation.

Lack of association of the angiotensin converting enzyme polymorphism with essential hypertension in a Chinese population.

To examine the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and essential hypertension in a Chinese population, a case-control study was conducted using 157 hypertensive and 115 normotensive subjects. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. Plasma ACE activity was determined using spectrophotometry. The difference of allele frequencies between normotensives and hypertensives was statistically significant (chi 2 = 4.467, P = .035), while the genotype distribution was not different between normotensive and hypertensive subjects (chi 2 = 3.954, P = .138). Plasma ACE activity was highest in the DD genotype, followed by the ID genotype, and the lowest in the II genotype (P = .0001 in normotensives and P = .163 in hypertensives, respectively). Thus, we conclude that the ACE gene polymorphism is not associated with essential hypertension in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.

Age- and gender-dependent association of the angiotensin-converting enzyme gene with essential hypertension in a Chinese population.

A case-control study was carried out on 272 Chinese subjects over 40 years of age, including 157 hypertensives and 115 normotensives, to examine the association between angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and blood pressure (BP) status. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. As a whole group, the difference of allele frequencies between normotensives and hypertensives was statistically significant (chi 2 = 4.46, P = 0.03; D/I odds = 1.46), while there was no difference in the genotype distribution (chi 2 = 3.95, P = 0.13). In a subgroup with elderly hypertension (age > 65), the frequencies of D-allele and DD genotype significantly increased (chi 2 = 4.43, P = 0.03 and chi 2 = 4.03, P = 0.08, respectively; D/I odds = 2.28). The association and relative risk increased further in the male gender (chi 2 = 6.65, P = 0.01 and chi 2 = 7.51, P = 0.02 respectively; D/I odds = 4.57 and DD/II odds = 12.00 respectively). The D-allele increased with age in the hypertensives, while the I-allele increased with age in normotensives. Thus, we conclude that the deletion polymorphism of the ACE gene is significantly associated with male elderly hypertension, at least in this Chinese population. This observation, if proved in a larger population, may have some implications for the prevention and treatment strategy for elderly hypertension.

Left isomerism in a middle-aged woman with early-onset atrial fibrillation.

An unusual case of left isomerism in a 52-year-old woman with early-onset atrial fibrillation was presented. Magnetic resonance imaging clearly delineated the morphology of both atrial appendages, the vascular anatomy and all other associated anomalies, obviating further invasive studies. The discovery of left isomerism at advanced age indicates that abnormal atrial situs itself is of less clinical importance, and despite the associated sinus node dysfunction may predispose the heart to atrial fibrillation.

Influence of isolated diastolic hypertension identified by ambulatory blood pressure on target organ damage.

Clinical decisions and controlled studies in regard to hypertension have long emphasized the casual diastolic blood pressure (DBP). The influence of superimposition of high systolic blood pressure (SBP) on the target organ damage has been less studied. To assess the role of isolated diastolic hypertension without interference of superimposition of systolic hypertension, 171 subjects with normal blood pressure, isolated diastolic hypertension (SBP < 140 and DBP > or = 90 mmHg) isolated systolic hypertension (SBP > or = 140 and DBP < 90 mmHg) or combined hypertension (SBP > or = 140 and DBP > or = 90 mmHg) determined by mean 24-h ambulatory blood pressure were compared in relation to target organ damage including ECG abnormality related to hypertension, cardiac enlargement by chest X-ray, proteinuria and retinopathy. The incidence of target organ damage was lower in subjects with normal BP than in the other three groups. The incidence of target organ damage was almost significantly higher in patients with isolated systolic hypertension than in those with isolated diastolic hypertension. No significant difference in the incidence of complications existed between patients with isolated systolic and combined hypertension. These findings demonstrate that the severity of hypertensive complications is more closely related to mean ambulatory SBP than mean ambulatory DBP. The level of systolic BP is important for predicting the severity of target organ damage in patients with high diastolic BP, because there is a significant difference in the incidence of target organ damage between isolated diastolic hypertension and combined hypertension.

Infundibular pulmonic stenosis with intact ventricular septum: a report of 15 surgically corrected patients.

Infundibular pulmonic stenosis with intact ventricular septum of primary origin is an uncommon condition. We report 15 such patients (nine males and six females, aged 7-36 years) who had undergone surgical correction for the anomaly during the period between 1975 and 1992. The occurrence of this clinical setting represents 0.19% (15/7826) of all cardiac operations and 0.46% (15/3222) of congenital heart diseases undergoing surgical correction during that period of time. The lesion was of discrete fibromuscular hypertrophy of the infundibulum in all 15 patients. The presenting symptoms of most patients were exertional dyspnea and syncope; however, five patients with severe obstruction were asymptomatic. The peak systolic pressure gradient across the infundibulum ranged from 71 to 230 mmHg. There was only one operative death; the remainder had remained well following the surgery over a mean follow-up period of 35 months. Surgical correction for infundibular pulmonic stenosis is rewarding in the absence of heart failure.

Circadian variations of atrial natriuretic peptide in normal people and its relationship to arterial blood pressure, plasma renin activity and aldosterone level.

To investigate the circadian variations of plasma atrial natriuretic peptide (ANP) and its relationship to arterial blood pressure, plasma renin activity and aldosterone level, we determined 24-h blood pressure in 14 healthy volunteers. Plasma ANP concentration, renin activity and aldosterone levels were measured every 3 h by radioimmunoassay. We found no significant circadian variation of plasma ANP level (pg/ml) (daytime level, 62 +/- 24 vs. nighttime level, 57 +/- 19, P = 0.146) and plasma renin level (ng/ml/h) (1.32 +/- 0.78 vs. 1.15 +/- 0.57, P = 0.148), but there was diurnal change of blood pressure (mmHg) (systolic, 122 +/- 7 vs. 116 +/- 11, P < 0.001; diastolic, 80 +/- 11 vs. 72 +/- 11, P = 0.025) and plasma aldosterone level (pg/ml) (86 +/- 42 vs. 62 +/- 37, P < 0.001). The blood pressure and aldosterone levels reached maxima (11:00 h and 08:00 h, respectively) before that of ANP (17:00 h) and then decreased together until the nadir at 02:00 h. This might indicate that elevation of arterial blood pressure and plasma aldosterone level stimulate release of ANP under normal physiological conditions.

Reappraisals of atrioventricular node reentrant tachycardia: lessons learned from surgical treatment.

The exact site of reentrant circuit involved in the atrioventricular node reentrant tachycardia was questioned. Seven patients (6 females and 1 male), aged 21 to 64 years (mean = 40 +/- 17 years), with refractory nodal reentry, underwent surgical treatment. The associated cardiac diseases included rheumatic valvar disease in two and an atrial septal defect. Electrophysiologic studies before surgery showed dual nodal pathways in 4 patients. Right atrial endocardial mapping was performed and the earliest retrograde atrial activation during tachycardia was mapped to the apex of the triangle of Koch in 6 patients and near the orifice of coronary sinus in one. Perinodal dissection was performed according to the location of earliest retrograde atrial activity. Care was taken to preserve as much of the atrioventricular node and its arterial supply as was possible. Immediately after surgery, conduction in an antegrade direction recovered and the tachycardia could no longer be reproduced. There was no surgical mortality or morbidity. At 10 to 26 months of follow-up, all patients remain free of tachycardia without antiarrhythmic drugs. Four patients underwent repeated electrophysiologic studies at 2 weeks to 6 months after surgery. Dual nodal pathways were no longer demonstrated. It is concluded that the perinodal atrial tissue plays a part in the atrioventricular nodal reentry, and that surgical dissection is a simple and effective treatment for patients with refractory atrioventricular node reentrant tachycardia.

Congenital mitral stenosis: challenge of percutaneous transvenous mitral commissurotomy.

A 26-year-old woman with congenital mitral stenosis and embolic stroke was referred to our hospital. The echocardiogram showed a hypoplastic posterior mitral valve leaflet with short, unbalanced chordal attachments to the posteromedial papillary muscle. The mitral valve area was 0.9 cm2 by the pressure half-time method. There was no left atrial thrombus and spontaneous echo contrast. Percutaneous transvenous mitral commissurotomy was performed since the suggestion of surgical management was refused by her family members. A rupture at the chordae tendinae of the hypoplastic posterior papillary muscle developed during the procedure and needed mitral replacement. We advise that percutaneous transvenous mitral commissurotomy be avoided in adult patients with congenital mitral stenosis having an asymmetric and hypoplastic mitral valve.

Ultrasonic tissue characterization evaluates myocardial viability and ischemia in patients with coronary artery disease.

To evaluate whether or not ultrasonic tissue characterization (UTC) can detect jeopardized or salvageable myocardium in patients having chronic coronary artery disease, we studied 103 patients with sequential UTC, dobutamine stress echocardiography (DSE) and (201)thallium stress-reinjection single-photon emission computed tomography (T1-SPECT). This revealed that the weighted amplitude of the cyclic modulation of integrated backscatter was larger for the myocardium with less ischemia burden or greater viability (p<0.001). The segments with larger ischemia burden or the nonviable myocardium demonstrated the contrary result. Using the receiver-operating characteristic curve analyses to determine the cutoff value of weighted amplitude for various predictions, UTC can detect ischemia in normokinetic myocardium (kappa = 0.34 compared to DSE or T1-SPECT) and viability in dyssynergic myocardium (kappa = 0.57 compared to DSE and 0.45, to T1-SPECT). These observations show that UTC may prove useful in the identification and pathophysiological understanding of myocardial ischemia and viability.

Q-T interval prolongation and pleomorphic ventricular tachyarrhythmia ('Torsade de pointes') in organophosphate poisoning: report of a case.

1. A 63-year-old woman presented with drowsy consciousness and dyspnea, followed by respiratory failure, after taking a bottle of parathion for suicide. 2. Sinus tachycardia was noted initially by ECG and Q-T interval prolongation with pleomorphic ventricular tachyarrhythmia ('Torsade de pointes') occurred on the third day of admission. 3. Torsade de pointes was relieved by magnesium sulfate and atropine sulfate intravenously. Q-T interval returned to normal on the fifth day of admission. 4. Practicing physicians should be aware of this uncommon type of cardiac toxicity caused by organophosphate poisoning, Q-T interval prolongation and pleomorphic ventricular tachyarrhythmia.